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Cardiac Troponin-TT levels in heart blood

Original Research Article

Cardiac Troponin-T
Troponin T levels in heart blood as a
marker to diagnose postmortem myocardial
infarction
B. Bheeshma1*, V. Geetha2, Jay Raju3, Sandhya Manohar4
1

Associate Professor, Department of Pathology, Gandhi Medical College, Hyderabad, India

Assistant Professor,, Department of Pathology, Gandhi Medicall College, Hyderabad, India
3
Professor, Department of Forensic Medicine, Gandhi
Gandhi Medical College, Hyderabad, India
4
Associate Professor,, Department of Forensic Medicine, Gandhi Medical College, Hyderabad, India
*Corresponding author email: bheeshma60@gmail.com
2

How to cite this article: B. Bheeshma, V. Geetha,

Geetha Jay Raju, Sandhya Manohar.
Manohar Cardiac Troponin-T
levels in heart blood as a marker to diagnose postmortem myocardial infarction
infarction. IAIM, 2015; 2(3):
108-118.

Available online at www.iaimjournal.com

Received on: 27-02-2015

Accepted on: 05-03-2015

Abstract
Cardiac deaths account for 50% of all deaths in developed and 25% in the developing world. OneOne
sixth of worlds population lives in India and heart disease accounts for 24% of all deaths. Sudden
death accounts for two-thirds
thirds of all autopsies in Forensic Medicine.
Medicine. Actual detection of histological
sequence of the infected myocardium will develop only after significant time of, between onsets of
myocardial infarction (MI) in death. Cardiac Troponin-TT is not normally present in serum unless
cardiac necrosis has occurred therefore cardiac Troponin levels
evels act as a specific and sensitive
indication of myocardial infarction. The present study was conducted on cases coming for medico
legal autopsy to the Forensic Medicine Department at Gandhi Medical College/Hospital,
College/Hospital Hyderabad,
Andhra Pradesh, India for a period of 1 year from January 2014 to December 2014. Total 12 cases
with 6 controls were analyzed. Cardiac Troponin-T
Troponin T Level was markedly elevated >2.000 ng/ml in all
except one case of suspected MI. Sensitivity was found
found to be 91.66% and specificity 66.66%.

Key words
Heart disease, Cardiac Troponin--T, Myocardial infarction.

Introduction
st

In 21 century, cardiac deaths accounted for

50% of all deaths in the developed and one
fourth in the developing world. It is accepted

universally that myocardial infarctions are fore

most killers and destroyers of mankind
manki
today
[1].. By 2020, heart disease will lead to 25 million
deaths all over the world annually [2]. One-sixth

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Cardiac Troponin-TT levels in heart blood

of worlds population lives in India and heart
disease accounts for 24% of all deaths [3]. Indian
people have been found to have the
unfortunate distinction of having the highest
prevalence of coronary artery disease among all
ethnic groups in the world, the projected rise in
the mortality rates (>100%) in the next 25 years
[4].
Sudden death accounts for approximately twotwo
thirds of autopsies in forensic medicine [5].
Natural death within 1 hour after the beginning
of acute symptoms is defined as sudden cardiac
death [6].. Due to ventricular fibrillation caused
by myocardial irritability induced by ischemia or
infarction. Acute myocardial infarction
infarctio (AMI) is a
serious and potentially lethal manifestation of
coronary artery disease, affecting more
m
than 7
million people worldwide
wide each year and proved
to be a cause of sudden death [7].
[7]
In postmortem examination of dead bodies
subjected to autopsy with probable sudden
cardiac death, a diagnosis of myocardial
infarction is usually made based on the finding
of severe atherosclerosis occlusive coronary
artery disease. Actual detection of histological
sequelae of the infracted myocardium will
develop, only after significant time lag between
onset of myocardial infarction and death [8].
Detectable loss of lactate dehydrogenase will be
seen 5 hours after infarction using enzyme histohisto
chemistry [9].
Recently several studies have shown keen
interest on the application
lication of biomarkers to
diagnose AMI.
The presence of cardiac
biomarkers in blood with increase sensitivity to
detect cardiac cell necrosis enables to diagnose
AMI in 1/3rd of patients who might not had
accomplished the criteria for diagnosis of
myocardial infarction [10].

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Troponin is a protein complex, situated on the
actin filament and regulates calcium mediated
interaction of actin and myosin filaments
filamen during
muscular contraction. It has three
th
subunits cTnI
(inhibitory), cTnT (Trophomyosin Binding) and
a
TnC (calcium Binding). Cardiac
ardiac Troponin T is the
double filament protein and predominantly this
protein is bound within myocytes, and less than
10% is dissolved in the cytosol [11].
Cardiac Troponin T is not normally present in the
serum unless cardiac cell necrosis has occurred.
Thus it is more cardiac specific. Recent studies
have shown that cardiac Troponin levels act as a
specific and sensitive indicator of myocardial
infarction [12].
nostic value of cardiac Troponin T is
The prognostic
most important as it is not dependent on age,
sex, ECG changes as well as levels of age old
biochemical markers such as Creatine Kinase
(CKMB). Cardiac Troponin T (cTnT)
(
is elevated in
all patients with acute myocardial
myocardia infarction
diagnosed by World Health Organization (WHO)
criteria. Increased levels of cardiac Troponin T
appears in the blood within 3-24
3
hours after AMI
depending on factors such as infarct size and
they can be estimated for up to 2 weeks in the
living [13].
The cardiac Troponin-TT assay is based on
monoclonal antibody system using a polypoly
(streptavidin)-biotin
biotin capture system with a
ruthenium complex cTnT in the blood sample or
plasma combines with both the biotinylated
anti-Cardiac
Cardiac Troponin T and anti-Cardiac
anti
Troponin T and antibody [14].
[14]
The European Society of Cardiology (ESC)/
(
American College of Cardiology (ACC)
(
guidelines
th
recommend using the 99 percentile of a
healthy population as a cut--off for AMI using an
assay with an acceptable precision.
An
acceptable precision has been defined as a coco

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Cardiac Troponin-TT levels in heart blood

efficient of variation < 10%.
For cardiac
th
Troponin T, the 99 percentile value of a healthy
population is 0.1ng/ml; however, the 10%
coefficient of variation requirement for the
usual assay was met at a higher
gher level (i.e. 0.3
ng/ml) [15].. In clinical practice, the cTnT assay
has been approved for the diagnosis of AMI with
high sensitivity and specificity [16].
[16]

Aim and objectives

To estimate postmortem cardiac

Troponin T levels in the heart blood to
diagnosee acute myocardial infarction in
autopsy.
To correlate cardiac Troponin T levels
with histopathological
istopathological diagnosis of acute
myocardial infarction in autopsy.

Material and methods

Present study was prospective study conducted
at Forensic Medicine Department, Gandhi
Medical College/Hospital, Andhra Pradesh,
Pradesh India
from January 2014 to December 2014.
Inclusion criteria
A sudden death, adult dead body with cause of
death unexplained by external examination
ex
(body was found
nd dead at home, outdoors
o
or in
the hospital emergencyy room). Autopsy was
done within 48 hours of death.
Exclusion criteria
Allll dead bodies subjected for autopsy
after 48 hours of death.
Dead bodies found to have septicemia,
renal disease, pulmonary embolism,
myopericardtis, and congestive heart
failure.
Dead bodies found to undergone cardiac
surgery
or
cardio
pulmonary
resuscitation or cardiac concussion.

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The internal autopsy was done for 12 sudden
death bodies and 6 controls consisting
cons
of deaths
due to poisoning,, stroke, Tuberculosis etc.
Hearts were exposed and blood was withdrawn
from the pericardial cavity, right and left
chamber of the heart with a 21G sterile syringe
with needle and immediately transferred to a
sterile sampling
ing anticoagulant added test tube
and sent for analysis at Department
epartment laboratory
lab
for the measurement of cardiac Troponin T
levels with cobase
base 232 SANDWICH Analyzer.
Analyz
Test principle
Sandwich principle and total time duration of
assay was 9 minutes.
Cobase 232 analyzers
1st incubation: 50 L of sample, a
biotinylated monoclonal anti-cardiac
anti
Troponin T-specific
specific antibody, and a
monoclonal anti-cardiac
cardiac Troponin TT
specific antibody labeled with a
ruthenium complex react to form a
sandwich complex.
2nd incubation: After adhesion of
streptavidin-coated
coated micro particles, the
complex becomes bound to the sold
phase via interaction of biotin and
streptavidin.
Cobase 232avec scanner
During a 9 minute incubation period, the
antigen in the sample (50 L),

a
biotinylated monoclonal anti-cardiac
anti
Troponin
T-specific
specific
antibody,
monoclonal anti-cardiac
cardiac Troponin TT
specific labeled with a ruthenium
complex and streptavidin-coated
streptavidin
micro
particles reacted to form a sandwich
complex, which wass bound to the solid
phase. The reaction mixture was seen in
strip method. Cardiac Troponin T levels
were above 2.000 ng/ml.
ng/

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Cardiac Troponin-TT levels in heart blood

The autopsy was followed by microscopic study.
study
Once the heart was removed it was
wa washed with
running water and weighed. Gross examination
of the entire heart was done to look for the
presence of scar due to old infarct then after
serial sections of coronary artery were made at
a distance of 3 mm to look for presence of
plaques or thrombus. Serial
erial transverse sections
involving full thickness of heart was made at
a a
distance of 1 cm each from the apex to
atrioventricular (AV) groove.
ve. Slices were
examined for old fibrotic scar and softening. All
the samples were sent for histopathological
h
examination. Histopathological diagnosis of
acute myocardial infarction was made
m
from
following criteria, which included wavy
myofibers, coagulative necrosis, ischemic
contraction, band necrosis, and polymorphous
infiltration into the interstium.

Results
The study and control sample contained 11 and
5 men respectively and one woman in each
group. The average age of the control sample
was 50 (48-56) years and the average age of the
cardiac death sample was 52 (44-60)
(44
years. In
the control sample, two patients died due to
acute organophosphorus
phosphorus poisoning. Three cases
died due to cerebro-vascular
vascular accident and or
metabolic encephalopathy, and one was due to
pulmonary tuberculosis. Cardiac Troponin T
level was markedly elevated (>2.000 ng/ml)
ng/
in all
except one case of suspected MI in the study
sample and also markedly elevated in the
t
control sample except two cases (probably due
to autolysis).
Histopathological examination (HPE) of the
hematoxylin and eosin stained, heart slices,
showed that four cases of the study group had
evidence of early myocardial infarction with
features off myonecrosis, waviness of fibers,
nucleomegaly,
pyknotic
nuclei
and
polymorphous infiltration. Three cases of acute

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MI deaths demonstrated, myocardium with
multiple foci of infarction showing
show
hyalinized
collagen fibers. In areas of old infarction, HPE
revealed
ealed evidence of dense fibrous tissue
replacing
cing normal myocardial tissue. Four of the
control cases showed mild eosinophilia of the
myocardial fibers with mild infiltration of
polymorphs.
Microscopic features of MI
The microscopic appearances of human
myocardial infarcts were
re complex as per Table 1.
Cardiac Troponin T concentration levels in heart
blood and pericardial fluid by highly sensitive
Cardiac Troponin T quantitative assay were as
per Table 2 and Table - 3.
Histopathological examination results were as
per Table 4 and Table - 5.
Sensitivity and specificity of cardiac Troponin T
in study and control groups

Sensitivity =

Total MI cases with positive cTnT

test/ HPE results____________
results
Total of all MI cases tested

Sensitivity = 1112 x 100 = 91.66%

Specificity =

Total non MI/healthy cases with

negative cTnT test/HPE results
Total of all healthy cases tested

Specificity = 46x100 = 66.66%

Discussion
World Health Organization (WHO)
(
defines
sudden death as those that occurs within 24
hours of onset of terminal illness. 80% of sudden
cardiac deaths are due to coronary
atherosclerosis. Establishment of cause of death

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Cardiac Troponin-TT levels in heart blood

in cases of sudden cardiac death is a challenging
task to the Forensicc Pathologist. Identification of
early myocardial infarction during autopsy pose
difficulty, as apparent gross change of infarction
takes 24 to 48 hours following occlusion of
major artery in humans [1].
Even though minimal microscopic evidence is
recognized
zed as early as 6 hours, in the absence of
gross changes the involved area may be missed
when random blocks are taken for histo
pathological examination. Very few studies are
conducted on human heart during autopsy for
detection of early myocardial infarction
infarc
[2]. The
rationale of using the measurement of a protein
in blood to detect injury to cells is
straightforward and requires consideration of a
few major factors as mentioned below [3].
[3]
Criteria for a blood marker of cell death
I.
Sensitivity
Abundance in cell
Location in cell
II.
Sample timing
Mode of entry into blood
Half-life
life of elimination
III.
Specificity
Distribution
tribution in different cells/organs
cells/
The myocyte is the major cell in the
myocardium, and the hearts action is to pump
blood. Because myocytes essentially cannot be
regenerated, if heart cells die, then cardiac
function has a high probability of being
impaired. When the cell dies, the proteins
prote inside
the cell will be released, with proteins in the
cytoplasm leaving the cell more rapidly than
ones in the membranes
mbranes or fixed cell elements.
The most sensitive markers should be those in
highest abundance in the cell, the proteins
involved in contraction
raction and producing the
energy to support it should be good candidates
for biomarkers of cardiac injury which
wh
could be
detected in blood. Also, one has to consider the

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means by which the
he markers can reach the
blood. Since occlusion of blood flow is the
primary
rimary cause of myocardial infarction, most of
the proteins reach the blood via the lymphatics
where they are prone for degradation leading if
the protein has a cardiac specific form.
fo
While
utilizing abundant cardiac proteins involved in
contraction or energy
rgy production seems
obvious, it is not exactly
tly the way the field
evolved. Today, we can identify candidate cell
injury markers via gene expression or
proteomics in a reasonably straightforward
manner. However, these are recent advances
which required sequencing
encing entire genomes and
the development of technologies which were
not available until recently.
The aim of this short study was to ascertain the
relationship of deaths due to acute MI between
cardiac
ardiac Troponin T levels and correlate
correl
them
with the HPE findings. Limitations of this study
included factors like cohort size, autolysis,
variation in time since death, and cold storage
duration. In spite of these shortcomings, the
data was analyzed that may help our
understanding of cardiac
ardiac Troponin T [6].
At the outset, it is inevitable that under normal
conditions almost all bodies subjected for
postmortem examination will demonstrate
some degree of autolysis and hemolysis which
will cause a rise of cardiac
ardiac Troponin T levels
above their premortem levels as free
hemoglobin interferes with assays for measuring
Troponin, CK, and CK-MB [7, 8].
In this study,, from only two cases of heart blood,
cTnT level from the control sample was within
normal range for living patients, while the
remaining samples showed high
hig levels, may be
due to autolysis that would be false positive of
AMI in a living patient similar to other studies
[16, 17].

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Cardiac Troponin-TT levels in heart blood

Others have reported levels similar to living
persons and have dismissed the role of
hemolysis and autolysis. Some have propounded
that cardiac
ardiac Troponin T levels may be elevated
in many deaths because of nonspecific cardiac
injury due to lack of oxygen during the agonal
period [18, 19].. Pericardial fluid bathes the
myocardium and some studies have shown
increased levels of cardiac
ardiac Troponin
T
T in
pericardial fluid when compared to peripheral
blood. Although
gh this was a small study, the
cardiac
ardiac Troponin T levels in heart blood of right
ventricle, left ventricle and pericardial fluid were
statistically significant. Cardiac arrhythmias
during
ring the ischemic period may play a key role in
sudden cardiac death, wherein, MI could not be
demonstrated [20, 21].
This study showed that there was
wa a strong
relationship
elationship between postmortem cardiac
c
Troponin T (cTnT) reactivity with death caused
by myocardial
rdial infarction correlating significantly
with histopathology findings. In this study
almost all values were above the normal range
for living patients.
Clinical uses of cardiac
ardiac Troponin-T
Troponin
Diagnosis of AMI (Acute Myocardial
Infarction)
Reperfusion detection
Infarct size estimation
Stratification of risk
Detecting peri operative myocardial
infarction
Troponins have proven value as prognostic
markers. In patients who have non-ST
non
segment
elevation acute coronary syndrome and who
were studied in the Thrombolysis
lysis in Myocardial
Infarction (TIMI) IIIB Trial, graded increase
increas in
Troponin I at baseline were significantly and
independently correlated with increasing
mortality.

Cardiac specific Troponins

Troponin is a protein complex consisting of the
three subunits namely Troponin T (TnT),
Troponin I (Tnl) and Troponin C (TnC) located on
the thin filament of striated muscles. Cardiac
specific Troponin T (cTnT) and cardiac specific
Troponin-II (cTnl) have amino acid
ac sequences
different from those of the skeletal muscle
forms of these proteins. Since cTnT and cTnl are
not normally detectable in the blood of healthy
individuals but may increase after ST segment
elevation MI (STEMI) to levels >20 times higher
than the upper reference limit (the noise level of
the assay), the measurement of cTnT or cTnl is
of considerable diagnostic usefulness and they
are now the preferred biochemical marker for
MI Levels start rising within 3-6
3 hours and peaks
by 24 hours and peaks by 24 hours. They remain
elevated for 7 to 10 days after STEMI.
Cardiac Troponins are
re superior to CKMB, as
follows.
Troponins are markedly cardiac specific
especially Cardiac Troponin I (100%).
Its marked increase and extended
duration of half life in the blood helps to
detect delayed cases of AMI.
Due to the cardiac specificity and their
very low concentration in serum of
normal individuals, cTns have greater
sensitivity for minor degrees of
myocardial injury.
In unstable angina cases, they are
effective prognostic
rognostic indicators than
CKMB.
A single level of cTnT in peripheral
blood after AMI can be used for
estimation of infarct size whereas CKMB
requires repeat samples.
Cardiac Troponin T versus cardiac Troponin I
Recently,
highly
sensitive
third
generation cTnT assays (hscTnT) are
highly cardiac specific with the overall

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Cardiac Troponin-TT levels in heart blood

diagnostic sensitivity, specificity and
efficiency
better
than
cTnI.
Standardization of cTnI assays is difficult
as it has many manufacturers with
varied results, whereas cTnT assay I
manufactured
factured by only one manufacturer
(Roche).
Other biochemical markers
Glycogen Phosphorylase (GPBB)
Of late, GPBB is one of the best markers for early
detection of AMI however it is also elevated in
UA when glycogen is broken.
History of biochemical marker
marke usage
myocardial injury was as per Table 6.

in

In the year 2000, the ESC/ACC guidelines

recognized the major role of biochemical
markers and made elevations in their levels the
key to diagnose AMI.
At that point of time, they had also recognized
and acknowledged that cTnT and cTnI had
surpassed Creatinine Kinase-MB
MB as the analytes
of choice for diagnosis.
Historical review of methods for detection of
early myocardial infarction in autopsy cases
Different methods have been discovered for
identification
n of early myocardial infarction
during autopsy. Every method has its own
advantages and limitations.
Many animal
experiments were conducted for detection of
early infarction. In the year 1960, histo chemical
staining using Tetrazolium dyes was introduced
as a method to identify early MI. Other methods
include Hematoxylin-basic
basic fuchsine-picric
fuchsine
acid
staining, Barbeito-Lopez
Lopez Trichrome staining,
measuring K+/Na+ ion ratio, Mg+/Ca+ ion ratio,
fluorescent microscopy, measurement of
sarcomere length and determination
determin
of density
of blood.

Conclusion
Forensic pathologistss seldom request Troponin
assay// test in the investigation of sudden cardiac
death because of firm diagnosis
iagnosis of cardiac death
as evident on gross autopsy and histological
findings coupled with significant symptoms.
However not all cardiac
diac deaths show these
finding e.g. Micro infarcts of the myocardium
may produce cardiac arrhythmias and
subsequent death. The search of a reliable
marker to support diagnosis of cardiac injury
was made by this study.
We also should be aware of the laboratorys
normal range, the elevated levels seen in
postmortem control samples, and the anatomic
site from which the sample is drawn. Although,
blood from central locations as the cardiac
ventricles and pericardial fluid
flu showed markedly
increased levels, they best equate anti-mortem
physiologic levels. Moreover, it is necessary to
correlate the laboratory reports with the place
of occurrence, history of the case, and HPE
findings. One issue with this study and studies
up to date is that cardiac
ardiac Troponin T levels are
tested in obvious patients with acute MI and
compared with patients who died of non cardiac
causes. Inevitably, all of these studies
st
concluded
that increased cardiac
ardiac Troponin T levels
correlate with the cause of death and supported
the gross and HPE findings.
ndings. Therefore more
large scale studies are needed before definite
conclusions can be drawn from these assays. It is
hoped that this study can be a foundation for
future larger studies.
The sensitive markers should be that highest
abundance in the cell. The major function of the
heart is contraction, the proteins involved in
contraction in producing the energy are
important biomarkers of cardiac injury which
could be detected in blood and cardio specific
proteins
ins like Cardiac Troponin T levels are more
sensitive and specific biomarkers.

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Cardiac Troponin-TT levels in heart blood

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Source of support: Nil

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ISSN: 2394-0034 (O)
cardiac death with regard to pathology.
Leg Med (Tokyo), 2006; 8(2): 94-101.
21. Heberden W. Some account of disorder
of the breast.
east. Medical transactions.
College
ge of Physicians in London, 1772; 2:
59.

Conflict of interest: None declared.

Table 1: Microscopic features of MI.

Time
0 to 30 minutes
30 minutes to 4 hours
4 to 12 hours
12 to 24 hours

1 to 3 days
3 to 7 days
7 to 10 days
10 to 14 days
2 to 8 weeks
>2 months

Light microscopic features

Nil changes
Usually no change; variable waviness of fibers at the border.
border
Early coagulation necrosis; edema; hemorrhage,
hemorrhage
Continuing coagulative necrosis; pyknosis of nuclei; myocytes hyper
eosinophilla; marginal contraction band necrosis; early neutrophil
infiltration.
Coagulation necrosis with loss of nuclei and striations; brisk neutrophil
infiltration.
Beginning of disintegration of dead myofibers with dying neutrophils; early
phagocytosis of dead cells by macrophages at the border.
Well developed phagocytosis of dead cells; early formation of granulation
tissue at margins
Well established granulation tissue with new blood vessels and collagen
deposition
Increased collagen deposition with decreased cellularity
Dense collagen scar

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ISSN: 2394-0026 (P)

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Cardiac Troponin-TT levels in heart blood

Table - 2: Cardiac Troponin T concentration levels in study group (n=12).

Sr. No.

P.M. No.

Cardiac Troponin T Levels (ng/ml) (> 0.2

ng/ml +ve result)
Postmortem
Interval
Left
Right
Pericardial
ventricle
ventricle
Fluid

1.

886/13

>2.000

>2.000

>2.000

8 hours

2.

887/13

>2.000

>2.000

>2.000

10 hours

3.

987/13

>2.000

>2.000

>2.000

19 hours

4.

1014/13

>2.000

>2.000

>2.000

16 hours

5.

1129/13

>2.000

>2.000

>2.000

16 hours

6.

1423/13

>2.000

>2.000

>2.000

12 hours

7.

1426/13

>2.000

>2.000

>2.000

17 hours

8.

1436/13

>2.000

>2.000

>2.000

5 hours

9.

2170/13

>2.000

>2.000

>2.000

12 hours

10.

2239/13

0.063

0.051

0.093

6 hours

11.

2303/13

>2.000

>2.000

>2.000

18 hours

12.

2308/13

>2.000

>2.000

>2.000

24 hours

International Archives of Integrated Medicine, Vol. 2, Issue 3, March, 2015.

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Inference

Markedly
increased
Markedly
increased
Markedly
increased
Markedly
increased
Markedly
increased
Markedly
increased
Markedly
increased
Markedly
increased
Markedly
increased
Normal
Markedly
increased
Markedly
increased

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ISSN: 2394-0034 (O)

Cardiac Troponin-TT levels in heart blood

Table - 3: Cardiac Troponin T concentration levels in control group (n=6).
Sr. No.

P.M. No.

Cardiac Troponin T levels (ng/ml) (>2.000 Postmortem

ng/ml +ve result)
Interval
Left Ventricle
Right
Pericardial
Ventricle
Fluid

1.

890/13

>2.000

>2.000

>2.000

30 hours

2.

894/13

>2.000

>2.000

>2.000

28 hours

3.

982/13

>2.000

>2.000

>2.000

40 hours

4.
5.

1010/13
1121/13

0.05
0.05

0.06
0.08

0.03
0.06

6 hours
8 hours

6.

1420/13

>2.000

>2.000

>2.000

36 hours

Inference

Markedly
increased
Markedly
increased
Markedly
increased
Normal
Normal
Markedly
increased

Table - 4: Histopathological examination results in Study group (n=12).

Sr. No.
1
2

Observations
Evidence of early myocardial infarction
Evidence of early myocardial infarction and old infarction

No. of cases
4
3

Evidence of old infarction

Normal myocardial histology no areas of infarction

Table - 5: Histopathological examination results in control group (n=6).

Sr. No.
1
2
3

Observations
Evidence of early myocardial infarction
Evidence of old infarction
Normal myocardial histology. No areas of infarction

No. of cases
Nil
2
4

Table 6: History of biochemical marker usage in myocardial injury.

Time period
Late 1950s
1960s
1970s
Late 1980s
Mid 1990s

Marker
Aspartate amino Transferase (AST, SGOT)
Creatine Kinase isoenzyme (CK-MB
(CK
activity)
Lactate
ctate dehydrogenase isoenzymes (ratio of LDH1 to LDH2)
Creatine
eatine Kinase-MB
Kinase
mass concentration
Troponin I, Troponin T

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